Phytotoxic hazards of NiO-nanoparticles in tomato: A study on mechanism of cell death

Journal Article

Musarrat, M. Faisal, Q. Saquib, A.A. Alatar, A.A. Al-Khedhairy, A.K. Hegazy, J. . 2013

• نوع عمل المنشور: KSU Research Work
• رابط المنشور على الويب: Phytotoxic hazards of NiO-nanoparticles in tomato: A study on mechanism of cell death
• المجلة \ الصحيفة: Journal of Hazardous Materials
• رقم العدد: 15 April 2013
• رقم الإصدار السنوي: 250–251
• الصفحات: 318–332

مستخلص المنشور

Nickel oxide nanoparticles (NiO-NPs) in the concentration range of 0.025–2.0 mg/ml were examined for the induction of oxidative stress, mitochondrial dysfunction, apoptosis/necrosis in tomato seedling roots, as an in vivo model for nanotoxicity assessment in plants. Compared to the control, catalase (CAT), glutathione (GSH), superoxide dismutase (SOD) and lipid peroxidation (LPO) in 2.0 mg/ml NiO-NPs treatments exhibited 6.8, 3.7, 1.7 and 2.6-fold higher activities of antioxidative enzymes. At 2.0 mg/ml, 122% and 125.4% increase in intracellular reactive oxygen species (ROS) and mitochondrial membrane potential (ΔΨm) of seedling roots confirmed the oxidative stress and mitochondrial dysfunction. Comet assay exhibited a significant increase in the number of apoptotic (21.8%) and necrotic (24.0%) cells in 2.0 mg/ml treatment groups vis-á-vis in control 7% apoptotic and 9.6% of necrotic cells were observed. Flow cytometric analysis revealed 65.7% of apoptotic/necrotic cell populations and 2.14-fold higher caspase-3 like protease activity were recorded in 2.0 mg/ml treatment groups. Ultrastructure analysis revealed NiO-NPs translocation, nuclear condensation, abundance in peroxisomes and degenerated mitochondrial cristae. The dissolution of Ni ions from NiO-NPs signifies its potential to induce cell death presumably by Ni ions, triggering the mitochondrial dependent intrinsic apoptotic pathway.